There is an established relationship between anterior cruciate ligament (ACL) injury and the development of osteoarthritis (OA). Following injury and surgical reconstruction, OA is reported in the medial compartment of the involved knee in 30 to 60% of patients within five to eight years. While increased muscle co-contraction often occurs in the unloaded knee, more detailed biomechanical analysis from our lab has shown that the involved knee undergoes unloading in the medial compartment. That is, the compressive joint contact force in the medial compartment of the involved knee is less than in the uninvolved knee during gait. The unloading is observed immediately after injury and is still quite pronounced at six months, but loading returns to normal two years after ACL reconstruction. However, differences in loading between impaired and unimpaired limbs at six months post-surgery is correlated with OA development 5 years post-surgery. In this study, we will examine the biomechanical and biochemical basis for this by studying people at 3 months, 6 months and 2 years following ACL reconstruction. In the first aim, we will explore the biomechanical basis of this unloading using EMG and gait analysis techniques, couple with the use of a biomechanical model that will allow joint contact force estimation. In Aim 2, quantitative magnetic resonance imaging of the knee will be used to discern biochemical changes in the cartilage during the post-surgery period (same three time points). T1? and T2 relaxation time quantification (indicative of glycosaminoglycan loss and decreased collagen matrix organization) will be performed for each limb. In Aim 3, we will examine the effect of knee loading differences on knee cartilage stress distribution, using a finite element model. This will enable us to determine how the loading and biochemical changes influence the pressure in the cartilage. We believe that these aims will enable us to understand the mechanisms governing knee unloading following ACL reconstruction and will enable us to make recommendations for clinical treatment paths to avoid subsequent OA development in this population.